Silencing N29 Regulated miR-193b-5p/TGFBR2 Axis to Mitigate the Progression of Cardiac Hypertrophy

IF 3.2 4区医学 Q2 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Journal of Gene Medicine Pub Date : 2024-12-12 DOI:10.1002/jgm.70002

Hao Wu, Xinshuang Wang, Jing Yu, Jiao Li, Zhenhua Ma, Xi Sheng, Han Yang, Liping Wei, Xin Qi

{"title":"Silencing N29 Regulated miR-193b-5p/TGFBR2 Axis to Mitigate the Progression of Cardiac Hypertrophy","authors":"Hao Wu, Xinshuang Wang, Jing Yu, Jiao Li, Zhenhua Ma, Xi Sheng, Han Yang, Liping Wei, Xin Qi","doi":"10.1002/jgm.70002","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>The study aimed to analyze differentially expressed lncRNAs in a model of cardiac hypertrophy, specially focusing on the molecular mechanisms of lncRNA NONMMUT023529 (lncRNA N29) in myocardial hypertrophy. Based on gene microarray results, RT-<i>q</i>PCR validation confirmed that lncRNA N29 was significantly upregulated in TAC-induced mice cardiac tissues. Echocardiographic assessments further verified that silencing lncRNA N29 led to a marked improvement in cardiac function, which aligned with the pathological findings revealed by H&E and Masson staining. Meanwhile, immunofluorescence staining results also confirmed that silencing lncRNA N29 effectively inhibited myocardial hypertrophy. Dual luciferase reporter assay and western blot results confirmed that lncRNA can mediate miR-193b-5p/TGFBR2 axis to regulate smad/2/3 expression and mitigate the progression of myocardial hypertrophy. Our findings suggested that the close association between the protective mechanism involving in the silencing lncRNA N29 in myocardial hypertrophy and miR-193b-5p/TGFBR2 axis. We identified that lncRNA N29 might act as a therapeutic target for the treatment of myocardial hypertrophy.</p>\n </div>","PeriodicalId":56122,"journal":{"name":"Journal of Gene Medicine","volume":"26 12","pages":""},"PeriodicalIF":3.2000,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Gene Medicine","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/jgm.70002","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOTECHNOLOGY & APPLIED MICROBIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

The study aimed to analyze differentially expressed lncRNAs in a model of cardiac hypertrophy, specially focusing on the molecular mechanisms of lncRNA NONMMUT023529 (lncRNA N29) in myocardial hypertrophy. Based on gene microarray results, RT-qPCR validation confirmed that lncRNA N29 was significantly upregulated in TAC-induced mice cardiac tissues. Echocardiographic assessments further verified that silencing lncRNA N29 led to a marked improvement in cardiac function, which aligned with the pathological findings revealed by H&E and Masson staining. Meanwhile, immunofluorescence staining results also confirmed that silencing lncRNA N29 effectively inhibited myocardial hypertrophy. Dual luciferase reporter assay and western blot results confirmed that lncRNA can mediate miR-193b-5p/TGFBR2 axis to regulate smad/2/3 expression and mitigate the progression of myocardial hypertrophy. Our findings suggested that the close association between the protective mechanism involving in the silencing lncRNA N29 in myocardial hypertrophy and miR-193b-5p/TGFBR2 axis. We identified that lncRNA N29 might act as a therapeutic target for the treatment of myocardial hypertrophy.

Abstract Image

查看原文本刊更多论文

抑制 N29 调控 miR-193b-5p/TGFBR2 轴以缓解心脏肥大的进展

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Journal of Gene Medicine 医学-生物工程与应用微生物

CiteScore

6.40

自引率

0.00%

发文量

审稿时长

6-12 weeks

期刊介绍： The aims and scope of The Journal of Gene Medicine include cutting-edge science of gene transfer and its applications in gene and cell therapy, genome editing with precision nucleases, epigenetic modifications of host genome by small molecules, siRNA, microRNA and other noncoding RNAs as therapeutic gene-modulating agents or targets, biomarkers for precision medicine, and gene-based prognostic/diagnostic studies. Key areas of interest are the design of novel synthetic and viral vectors, novel therapeutic nucleic acids such as mRNA, modified microRNAs and siRNAs, antagomirs, aptamers, antisense and exon-skipping agents, refined genome editing tools using nucleic acid /protein combinations, physically or biologically targeted delivery and gene modulation, ex vivo or in vivo pharmacological studies including animal models, and human clinical trials. Papers presenting research into the mechanisms underlying transfer and action of gene medicines, the application of the new technologies for stem cell modification or nucleic acid based vaccines, the identification of new genetic or epigenetic variations as biomarkers to direct precision medicine, and the preclinical/clinical development of gene/expression signatures indicative of diagnosis or predictive of prognosis are also encouraged.